嗜酸粒细胞性支气管炎(EB)是一种独立的疾病吗?答案是否定的，现有的证据也不支持。 广义的EB是指气管和支气管壁存在明显嗜酸粒细胞浸润的一种病理状态，为描记气道炎症特征的术语。作为一种常见的发病机制，EB参与多种呼吸系统疾病的发生。哮喘的基本特点就是EB，并与气道高反应性、气道重塑和可逆性气道阻塞密切相关 。除此之外，非哮喘性EB(nonasth— matic eosinophilic bronchitis)、COPD、上气道咳嗽综合征和胃食管反流性咳嗽等均可见EB改变，甚至无下呼吸道症状的变应性鼻炎或部分健康人也存在这种类型的气道炎症。因此，EB在临床上至少存在哮喘、非哮喘性EB、合并COPD 和无症状等表现形式。广义的EB并不是一种疾病，而是多种呼吸道疾病的共同病理过程。 狭义的EB即非哮喘I生EB，是指以咳嗽为唯一症状、肺通气功能和气道反应性正常、诱导痰中嗜酸粒细胞明显增多而皮质激素治疗有效者，是慢性咳嗽的常见病因。目前有观点认为，和咳嗽变异型哮喘相似，EB可能是极轻微的哮喘或哮喘的前期表现。研究发现，EB的病因和发病机制与哮喘很相似。如引起哮喘的环境职业因素和吸入过敏原均可导致EB，Th2炎症反应是两者嗜酸粒细胞气道炎症的主要基础。大部分研究显示介导EB和哮喘的嗜酸粒细胞气道炎症的细胞和细胞因子相同，或仅有程度上的差别。EB和哮喘一样也存在呼出气一氧化氮浓度增加，气道上皮基底膜增厚和上皮下纤维化，气道炎症及气道重塑改变程度两者也相似 。最大的不同在于肥大细胞在气道壁不同部位的浸润和激活。哮喘患者肥大细胞主要浸润支气管平滑肌层，而在EB则主要位于支气管黏膜层 。肥大细胞在气道壁的不同空间分布可以解释哮喘的气道高反应性和EB的咳嗽高敏感性，但不足于据此认为两者为不同的疾病。
Objective To explore the effect of lower airway inflammation on the pathogenesis of upper airway cough syndrome( UACS) . Methods Ten cases of UACS and 10 cases of chronic rhinitis or sinusitis without cough were enrolled as group A and group B, respectively. And 10 healthy volunteers were included as controls( group C) . The cough threshold C2 and C5 to inhaled capsaicin, defined as the lowest concentration of capsaicin required to induce ≥2 and ≥5 coughs, was measured. The total and differential cell counts was determined in induced sputum, and the levels of histamine and prostaglandin E2 were analyzed in supernatant of sputum. Results Cough threshold was significantly lower in group A than group B [ C2: ( 0.65 ±0. 08) μmol / L vs ( 3.90 ±1. 37) μmol / L; C5: ( 1.59 ±0. 28) μmol / L vs ( 33.46 ±23. 71) μmol / L, P lt;0. 05] and comparable between group B and group C( P gt; 0. 05) . Group A, similar to group B( P gt; 0. 05 ) , contained more inflammatory cells, with decreased percentage of macrophages and increased percentage of neutrophils in induced sputum than group C( P lt; 0. 05) . Furthermore, the levels of histamine[ ( 9. 55 ±1. 89) ng/mL vs ( 2. 37 ±0. 25) ng/mL, P lt; 0. 05] and prostaglandin E2 [ ( 361. 71 ±39. 38) pg/mL vs ( 144. 34 ±15. 69) pg/mL, P lt; 0. 05] were higher in supernatant of induced sputum from group A than group B, while the latter was not different from group C( P gt; 0. 05) . Conclusion Increased cough sensitivity caused by airway inflammation may be important for the pathogenesis of UACS, and the activation of mast cells in mucosa of lower airway might be an important factor.